Environment-Neuroendocrine Interactions in the Control of Amphibian Metamorphosis

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The profound morphological changes which occur during amphibian metamorphosis are controlled by thyroid hormone, the production of which is regulated by the ncurocndocrine system. Attempts to identify neurohormones which control the tadpole thyroid axis have focussed on the tripcptide thyrotropin-releasing hormone (TRH). However, exogenous TRH does not influence the rate of metamorphosis or stimulate the release of thyrotropic activity (TSH) by tadpole pituitaries in vitro. We found that corticotropin-releasing hormone (CRH) is a potent stimulator of the thyroid axis in tadpoles and this led us to hypothesize that CRH may function as a common neuroregulator of thyroid and interrenal activity during metamorphosis (DENVER & LICHT, 1989). We and others have since demonstrated that injection of CRH-like peptides accelerates metamorphosis in several amphibian species and elevates whole body concentrations of corticosterone, thyroxine and triiodothyronine. Conversely, treatment with anti-CRH serum or a CRH receptor antagonist blocks or slows metamorphosis. Expression of the CRH gene is correlated with thyroid hormone production and morphogenesis. The activity of CRH neurons is extremely sensitive to fluctuations in the environment, and changes in the larval habitat can influence the rate of morphogennesis. We have evidence that CRH is involved in the acceleration of metamorphosis in a toad which undergoes rapid development in response to habitat desiccation. This response can be replicated in the laboratory, and treatment of tadpoles with CRH receptor antagonist blocks this response. The CRH neuron may function as a transducer of environmental information (e.g., environmental 'stress') during development and allow tadpoles to assess habitat quality and alter their rate of development accordingly.